What Is Avascular Necrosis?
Bone is the basic framework of the body. Bones provide the body the stability it requires for normal functioning and allows an individual to carry out activities without any problems. The bone in our body is a growing material meaning that it is constantly breaking down and getting renewed. Bones have protein in them and its outer layer is covered with nerves and blood vessels. Avascular Necrosis is a condition in which the blood supply to a bone, usually of the hips, is cut off and the bone starts to disintegrate as the blood required for new bone formation is no longer available to the bone.
This imbalance reaches such a stage that the rate of bone breakdown is far more than the rate of new bone formation, ultimately leading to collapse of the bone, and the joint stops functioning normally. There is deformity of the joint. This results in inflammation or in other words arthritis causing acute pain and difficulty functioning.
As stated, Avascular Necrosis usually affects the hip, as the hip joint has only one blood vessel that supplies blood to the bone. If this vessel gets damaged as a result of an accident or for reasons delineated below then it results in development of Avascular Necrosis.
This condition is quite rare and affects around 25,000 people on an average every year in the United States. The symptoms of this condition start to show up in both males and females in their fourth decade of life. Studies have shown that HIV positive individuals are more prone than the normal population to Avascular Necrosis.
What Causes Avascular Necrosis?
As stated, Avascular Necrosis is caused as a result of loss of blood supply to the bone. This blood supply may be cut off as a result of an accident during which the blood vessel supplying blood to the bone gets damaged and the blood supply is cut off. A bone fracture or a dislocation of the bone may also result in damage to the nerves and blood vessels. Individuals who are HIV positive tend to get Avascular Necrosis more than the normal population for unknown reasons. There are also certain medical conditions which reduce the blood supply to the bones. There are cases in which fat deposition in the blood vessels leads to loss of blood supply to the bone. Excessive use of steroids and alcohol can also lead to development of Avascular Necrosis.
Can Avascular Necrosis Heal On Its Own?
The answer to this question is in majority of cases Avascular Necrosis does not heal on its own. The cases in which Avascular Necrosis can heal on its own are among people who are used to taking excessive steroids or abuses alcohol and stopping its use results in natural healing of the blood vessel and regular supply of blood can be restored with time. Avascular Necrosis resulting out of fracture or an accident can also heal naturally once the fracture is treated. Other than this, there is no evidence to suggest that Avascular Necrosis heals on its own. In fact this is a condition which if not treated on time may progress to bone collapse which is extremely challenging for a physician to treat and ultimately the patient may require surgery in the form of core decompression to treat Avascular Necrosis.
The usual treatment for Avascular Necrosis is medications like Fosamax, putting less pressure on the affected joint, increased intake of calcium to make the bone strong, and ultimately surgical procedure in the form of a core decompression where a segment of the affected bone is removed to improve blood supply to the bone.
In extremely advanced cases, the surgeon may completely remove the affected bone and realign the bone in such a way that the joint surface which bears the weight of the body is supported by healthy bone and the individual may function normally despite having had Avascular Necrosis.
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- Zhao, D. W., Yu, M., Hu, K., Wang, W. J., Yang, L., & Guo, C. A., et al. (2015). Autologous Bone Marrow Mesenchymal Stem Cells Associated with Core Decompression for Treatment of Avascular Necrosis of the Femoral Head: A 5-Year Follow-Up Study. Stem Cell Research & Therapy, 6, 104. doi: 10.1186/s13287-015-0098-8
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